Further preclinical testing demonstrated that H3B‐8800 also selectively affected splicing factor mutant myeloid neoplasms by causing enhanced retention of GC‐rich introns in splicing factor mutant cells that are enriched in genes encoding spliceosomal proteins themselves.32 Ongoing efforts will be described later but a deeper understanding of the molecular targets of known inhibitors and their effects on splicing will help set the stage for this discussion. This evidence concerns the gene SLU7 and myeloid neoplasm.